Elective Laparoscopic Cholecystectomy as an Entrustable Professional Activity (EPA) for General Surgical Trainees in Australia.

Introduction: To evaluate the operation time and surgical outcomes of elective laparoscopic cholecystectomy performed by surgical trainees at different levels of training at Eastern health and hence, to establish the efficacy and safety of elective laparoscopic cholecystectomy as an Entrustable Professional Activity for surgical trainees in general surgery.

Objective: Elective laparoscopic cholecystectomies performed at our institution between January 2018 and January 2019 were included. Analyses were divided among three groups - consultants (C), fellows (F) and registrars (R).

Chemotherapeutic agents induce mitochondrial superoxide production and toxicity but do not alter respiration in skeletal muscle in vitro.

Chemotherapeutic agents (CAs) can independently promote skeletal muscle dysfunction, fatigue and wasting with mitochondrial toxicity implicated as a possible mechanism. Thus, we aimed to characterise the effects of various CAs on mitochondrial function, viability and oxidant production in C2C12 myoblasts and myotubes. All CAs significantly reduced the viable mitochondrial pool but did not affect mitochondrial functional parameters.

BGP-15 Protects against Oxaliplatin-Induced Skeletal Myopathy and Mitochondrial Reactive Oxygen Species Production in Mice.

Chemotherapy is a leading intervention against cancer. Albeit highly effective, chemotherapy has a multitude of deleterious side-effects including skeletal muscle wasting and fatigue, which considerably reduces patient quality of life and survivability. As such, a defense against chemotherapy-induced skeletal muscle dysfunction is required.

Mitochondria: Inadvertent targets in chemotherapy-induced skeletal muscle toxicity and wasting?

Chemotherapy has been associated with increased mitochondrial reactive oxygen species production, mitochondrial dysfunction and skeletal muscle atrophy leading to severe patient clinical complications including skeletal muscle fatigue, insulin resistance and wasting. The exact mechanisms behind this skeletal muscle toxicity are largely unknown, and as such co-therapies to attenuate chemotherapy-induced side effects are lacking. Here, we review the current literature describing the clinical manifestations and molecular origins of chemotherapy-induced myopathy with a focus on the mitochondria as the target organelle via which chemotherapeutic agents establish toxicity.